Researchers here describe chronic kidney disease as essentially an accelerated form of mitochondrial damage as described in the mitochondrial free radical theory of aging: "Chronic kidney disease (CKD) has been linked to oxidative stress caused by dysregulation of the genes that control mitochondria. A study [has] revealed alterations in respiration gene expression in the white blood cells of CKD patients. ... The researchers found 44 genes that were up-regulated in the peripheral blood mononuclear cells of CKD patients, compared to normal controls. Of these, 11 were genes were involved in the oxidative phosphorylation system. Further tests revealed that the levels reactive oxygen species (ROS) were significantly higher in the CKD group. [Researchers] suggest that these species are part of a vicious circle of respiration dysregulation that ultimately results in CKD ... Our hypothesis is that an increased production of ROS, due to the effect of pro-inflammatory mediators, may cause a profound inhibition of the oxidative phosphorylation system leading to a compensatory 'hypertrophy' of its components. In addition, a hypertrophic and impaired oxidative phosphorylation system may prime a vicious circle, causing a continuous release of ROS."